TY - JOUR
T1 - Usefulness of Lipoprotein-Associated Phospholipase A 2 Activity and C-Reactive Protein in Identifying High-Risk Smokers for Atherosclerotic Cardiovascular Disease (from the Atherosclerosis Risk in Communities Study)
AU - Tibuakuu, Martin
AU - Kianoush, Sina
AU - DeFilippis, Andrew P.
AU - McEvoy, John W.
AU - Zhao, Di
AU - Guallar, Eliseo
AU - Ballantyne, Christie M.
AU - Hoogeveen, Ron C.
AU - Blaha, Michael J.
AU - Michos, Erin D.
N1 - Funding Information:
Sources of Funding: This analysis was supported by funding from the American Heart Association Tobacco Regulation and Addiction Center (A-TRAC, NIH 1 P50 HL120163 ), a member of the Food and Drug Administration (FDA) Tobacco Centers of Regulatory Science for Research Relevant to the Family Smoking Prevention and Tobacco Control Act (P50). The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute , National Institutes of Health , Department of Health and Human Services , under Contract nos. ( HHSN268201700001I , HHSN268201700003I , HHSN268201700005I , HHSN268201700004I , HHSN2682017000021 ). Dr. Michos and Dr. Zhao were supported by the Blumenthal Scholars Fund for Preventive Cardiology Research . Dr. Hoogeveen received a research grant from diaDexus , which provided reagents to conduct the LpPLA2 activity assays. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the FDA.
Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2018/5/1
Y1 - 2018/5/1
N2 - Despite the causal role of cigarette smoking in atherosclerotic cardiovascular disease (ASCVD), the underlying mechanisms are not fully understood. We evaluated the joint relation between smoking and inflammatory markers with ASCVD risk. We tested cross-sectional associations of self-reported smoking status (never, former, current) and intensity (packs/day) with lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) activity and high-sensitivity C-reactive protein (hsCRP) in 10,506 Atherosclerosis Risk in Communities participants at Visit 4 (1996 to 1998). Using Cox hazard models adjusted for demographic and traditional ASCVD risk factors, we examined the associations of smoking status and intensity with incident adjudicated ASCVD events (n = 1,745 cases) over an average of 17 years, stratified by Lp-PLA 2 and hsCRP categories. Greater packs/day smoked was linearly associated with higher levels of both Lp-PLA 2 and hsCRP among current smokers. Compared with never smokers, the hazard ratio for incident ASCVD in current smokers was 2.04 (95% CI 1.76 to 2.35). Among current smokers, the risk for ASCVD per 1 pack/day greater was 1.39 (1.10 to 1.76). Both Lp-PLA 2 activity ≥253 nmol/min/ml and hsCRP >3 mg/L identified current smokers at the highest risk for incident ASCVD, with similar hazard ratios. hsCRP risk-stratified current smokers better based on intensity. Among current smokers, hsCRP improved ASCVD prediction beyond traditional risk factors better than Lp-PLA 2 (C-statistic 0.675 for hsCRP vs 0.668 for Lp-PLA2, p = 0.001). In this large cohort with long follow-up, we found a dose-response relation between smoking intensity with Lp-PLA 2 activity, hsCRP, and ASCVD events. Although both Lp-PLA 2 activity and hsCRP categories identified high risk among current smokers, hsCRP may better stratify risk of future ASCVD.
AB - Despite the causal role of cigarette smoking in atherosclerotic cardiovascular disease (ASCVD), the underlying mechanisms are not fully understood. We evaluated the joint relation between smoking and inflammatory markers with ASCVD risk. We tested cross-sectional associations of self-reported smoking status (never, former, current) and intensity (packs/day) with lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) activity and high-sensitivity C-reactive protein (hsCRP) in 10,506 Atherosclerosis Risk in Communities participants at Visit 4 (1996 to 1998). Using Cox hazard models adjusted for demographic and traditional ASCVD risk factors, we examined the associations of smoking status and intensity with incident adjudicated ASCVD events (n = 1,745 cases) over an average of 17 years, stratified by Lp-PLA 2 and hsCRP categories. Greater packs/day smoked was linearly associated with higher levels of both Lp-PLA 2 and hsCRP among current smokers. Compared with never smokers, the hazard ratio for incident ASCVD in current smokers was 2.04 (95% CI 1.76 to 2.35). Among current smokers, the risk for ASCVD per 1 pack/day greater was 1.39 (1.10 to 1.76). Both Lp-PLA 2 activity ≥253 nmol/min/ml and hsCRP >3 mg/L identified current smokers at the highest risk for incident ASCVD, with similar hazard ratios. hsCRP risk-stratified current smokers better based on intensity. Among current smokers, hsCRP improved ASCVD prediction beyond traditional risk factors better than Lp-PLA 2 (C-statistic 0.675 for hsCRP vs 0.668 for Lp-PLA2, p = 0.001). In this large cohort with long follow-up, we found a dose-response relation between smoking intensity with Lp-PLA 2 activity, hsCRP, and ASCVD events. Although both Lp-PLA 2 activity and hsCRP categories identified high risk among current smokers, hsCRP may better stratify risk of future ASCVD.
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U2 - 10.1016/j.amjcard.2018.01.020
DO - 10.1016/j.amjcard.2018.01.020
M3 - Article
C2 - 29525060
AN - SCOPUS:85042905277
SN - 0002-9149
VL - 121
SP - 1056
EP - 1064
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 9
ER -